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Circulatory Responses to Exercise

Berry College - Dept. of Kinesiology
by

David Elmer

on 17 January 2014

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Transcript of Circulatory Responses to Exercise

pulmonary circuit
systemic circuit
Organs
Muscles
Arteries
Arterioles
Capil
laries
Venules
Veins
*all exchanges of nutrients happens in
To compensate for increased oxygen demand during exercise:
cardiac output
blood sent to working muscles
blood flow to the cardiac cells is vital due to high oxygen demand, even at rest
if blood flow is blocked for even a few minutes, it can result in permanent damage to the heart
HEART ATTACK (myocardial infarction)
Differences between cardiac and skeletal muscle
cardiac:
involuntary contraction
shorter, branched
homogeneous
no satellite cells = no regeneration
intercalated discs - leaky membranes, transmit electrical signals
skeletal:
voluntary contraction
longer, no branching
heterogeneous
satellite cells
no intercalated discs
when a cell is signalled to contract, all the cells around it will contract as well
Cardiac cycle
cycle of contraction and relaxation
systole
diastole
ejects about 2/3 of the venticular blood volume
allows ventricles to fill with blood
Pressure changes:
70% of atrial blood flows directly to ventricle
30% is pumped in by atria
small increase in ventricular pressure
when ventricle contracts:
closes atrioventricular valves (prevents backflow)
opens pulmonary and/or aortic valves
once ventricular pressure exceeds arterial pressure
atrioventricular valves closing
pulmonary/aortic valves closing
Arterial blood pressure
force exerted by blood against arterial walls
systolic:
pressure during ventricular contraction
diastolic:
pressure during ventricular relaxation
120
80
mmHg
mmHg
Mean arterial pressure
MAP = diastolic + 0.33(systolic - diastolic)
pulse pressure
ex:
80
+
0.33(
120
-
80
)
=
80 13
+
=
93
mmHg
*only works at rest
Dangers of high arterial pressure
aka "high blood pressure" or hypertension
increased work of left ventricle results in hypertrophy (enlargement) of the myocardium
can result in reduced pumping capacity and heart failure
increased risk of heart attacks
increased risk of kidney damage
increased risk of rupturing cerebral blood vessel (stroke)
stroke volume
Vascular resistance
difference in arterial pressure and right atrial pressure creates for blood to circulate
driving pressure
=
length x viscosity
radius
4
HUGE increase in resistance from small decrease in radius
immune system
clotting
oxygen transport
via hemoglobin
"watery"
carries ions, proteins, hormones, etc.
influences blood viscosity
Electrocardiogram
ECG
aka EKG
allows for detection & determination of electrical problems in the heart
atrial depolarization
depolarization of ventricles
(hides atrial repolarization)
~.10 sec
ventricular repolarization
pressure
resistance
=
BLOOD FLOW
Heart Rate
controlled by the SA node
"pacemaker of the heart"
influenced by:
parasympathetic
sympathetic
nerve system
nerve system
vagus nerve
hyperpolarizes SA and AV nodes
slows heart rate
"parasympathetic tone"
increased tone = decreased heart rate
decreased tone = increased heart rate
responsible for initial increase in HR up to about 100 bpm
cardiac accelerator nerves
stimulates SA node and ventricles
release norepinephrine, binds to beta-receptors
increases heart rate and force of contraction
balanced by
cardiovascular control center
in the
medulla oblongata
sensitive to:
blood pressure
receptors in carotid arteries, arch of aorta, and right atrium
blood oxygen tension
body temperature
Heart Rate Variability
time interval between heart beats
R-R distance
the wider the range of variability, the better
indicates healthy balance between sympathetic and parasympathetic input
low variability indicates imbalance in regulation
risk factor for future cardiovascular disease
heart failure
myocardial infarction
hypertension
"sympathovagal balance"
X
Stroke Volume
amount of blood ejected by the heart per beat
3 variables:
Preload
Afterload
Contractility
end-diastolic volume
average aortic blood pressure
strength of ventricular contraction when preload and afterload are held constant
primary variable is
venous return
increased return, increased preload, increased stroke volume
3 mechanisms:
Venoconstriction
limits how much blood can be stored in the veins
sympathetic
constriction of smooth
muscle in veins
controlled by
cardiovascular control center
Muscle pump
rhythmic skeletal muscle contractions force blood back to the heart
isometric contractions will limit venous return
Respiratory pump
inspiration causes pressure drop in thorax and pressure increase in abdomen
draws/forces blood into thorax and towards the heart
pressure in ventricle must exceed pressure in aorta in order to eject blood
greater aortic or mean arterial pressure results in a decrease in stroke volume
influenced by catecholamines and direct sympathetic stimulation of the heart
epinephrine
norepinephrine
cardiac accelerator nerves
Frank-Starling law:
greater preload increases the strength of contraction of the ventricles
cardiac fibers lengthen, allowing more actin-myosin interaction
Greater venous return, greater stroke volume
CARDIAC OUTPUT
= HR x SV
Arterioles
Venules
70 kg, active (but untrained) college-aged male
no plateau in highly-trained people
WHY NOT?
increased venous return
improved ventricular filling
increased force of contraction (Frank-Starling)
decline in max heart rate with age results in decreased max cardiac output too
HRmax = 220 - age
+
-
12 beats
adults:
children:
HRmax = 208 - 0.7*age
trained athletes also tend to have lower maximal heart rates compared to untrained counterparts
Fick equation:
VO = Q x a-vO d
2
.
.
-
2
how much blood is coming through?
how much oxygen is in this blood?
minus
how much oxygen is in that blood?
central
peripheral
*pumping more blood and extracting more oxygen will both raise VO
2
to organs
to skeletal muscles
high resistance at rest (vasoconstriction)
at start of exercise -
autoregulation
increase metabolic rate during exercise
results in less oxygen within muscle as it gets used up
decreased oxygen tension
greater difference between oxygen concentrations inside/outside the muscle
increased CO tension
2
decreased pH
increased NO, K , and adenosine
+
"vasodilate!"
may also open capillaries that are normally closed at rest
50-80% of capillaries
amount of vasodilation depends on metabolic need of the muscle
sympathetic stimulation from exercise causes vasoconstriction
Circulatory responses to exercise
emotional influence
increased heart rate
increased blood pressure

compared to psychologically neutral environment...
rest-to-exercise
exercise-rest
if exercise is submaximal, plateau in 2-3 min
trained athletes recover more quickly after exercise
recovery takes longer the more intense and the exercise and the longer in duration the exercise is
Incremental exercise
Arm vs Leg exercise
Intermittent exercise
Prolonged exercise
heart rate and Q increase in direct proportion to oxygen uptake
ensures supply of oxygen increases to meet demand, up to a point...
increase in Q comes from decreased vascular resistance and increased blood pressure
increased workload for heart
double product:
heart rate x systolic blood pressure
very useful for prescribing exercise for people with cardiovascular or coronary heart disease
greater increase in blood pressure with arm vs leg exercise
greater increase in HR with arm vs leg exercise
probably linked to greater sympathetic outflow
smaller active muscle mass = less vasodilation = greater systemic resistance
recovery between bouts depends on variety of factors:
fitness
environment
duration
intensity
better fitness, faster recovery
cooler environment, faster recovery
shorter work intervals, longer rest, more complete recovery
lower intensity, faster recovery
cardiac output maintained
stroke volume declines
heart rate increases
cardiovascular drift
required for exercise at a given intensity
dehydration reduces plasma volume
makes up for less blood per beat
Regulation of cardiovascular adjustments
central command theory
1. changes at beginning of exercise initiated by motor signals
2. cardiovascular response is then regulated by peripheral feedback
central
peripheral
heart mechanoreceptors
muscle mechanoreceptors and chemoreceptors
carotid and aortic baroreceptors
1
1
2
2
2
1
1
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